IL-13 signaling through the IL-13α2 receptor is involved in induction of TGF-β1 production and fibrosis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2006-01

AUTHORS

Stefan Fichtner-Feigl, Warren Strober, Koji Kawakami, Raj K Puri, Atsushi Kitani

ABSTRACT

Interleukin (IL)-13 is a major inducer of fibrosis in many chronic infectious and autoimmune diseases. In studies of the mechanisms underlying such induction, we found that IL-13 induces transforming growth factor (TGF)-beta(1) in macrophages through a two-stage process involving, first, the induction of a receptor formerly considered to function only as a decoy receptor, IL-13Ralpha(2). Such induction requires IL-13 (or IL-4) and tumor necrosis factor (TNF)-alpha. Second, it involves IL-13 signaling through IL-13Ralpha(2) to activate an AP-1 variant containing c-jun and Fra-2, which then activates the TGFB1 promoter. In vivo, we found that prevention of IL-13Ralpha(2) expression reduced production of TGF-beta(1) in oxazolone-induced colitis and that prevention of IL-13Ralpha(2) expression, Il13ra2 gene silencing or blockade of IL-13Ralpha(2) signaling led to marked downregulation of TGF-beta(1) production and collagen deposition in bleomycin-induced lung fibrosis. These data suggest that IL-13Ralpha(2) signaling during prolonged inflammation is an important therapeutic target for the prevention of TGF-beta(1)-mediated fibrosis. More... »

PAGES

99-106

Journal

TITLE

Nature Medicine

ISSUE

1

VOLUME

12

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm1332

    DOI

    http://dx.doi.org/10.1038/nm1332

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1040901420

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/16327802


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